Production of nitric oxide in mouse peritoneal macrophages after priming with interferon-γ by the stem of Sinomenium acutum

The present study demonstrates that the aqueous extract of Sinomenium acutum stem (SSAE) produces nitric oxide (NO) upon treatment with recombinant interferon γ (rIFN-γ) in mouse peritoneal macrophages. Apparently SSAE has no effect on NO production by itself. This production is dependent on L-arginine and can be inhibited by the L-arginine analogue N(G)-monomethyl-L-arginine. The increased production of NO from rIFN-γ plus SSAE-stimulated cells was decreased by the treatment of protein kinase C inhibitor. Tumor necrosis factor-α (TNF-α) has been shown to stimulate the oxidative metabolism of L-arginine to produce NO. Mouse peritoneal macrophages secrete high levels of TNF-α after incubation with rIFN-γ plus SSAE. In addition, SSAE-induced NO production is progressively inhibited by anti-murine TNF-α neutralizing antibody. These results show that the capacity of SSAE to increase NO production from rIFN-γ-primed mouse peritoneal macrophages is the result of SSAE-induced TNF-α secretion. Copyright (C) 1999 Elsevier Science Ireland Ltd.